Kripke M L
Department of Immunology, University of Texas M.D. Anderson Cancer Center, Houston 77030.
Cancer Res. 1994 Dec 1;54(23):6102-5.
The carcinogenic activity of solar radiation has been known for nearly a century. However, within the past few years, we have realized that exposing the skin to sunlight also has profound immunological effects on the host and that these immunological changes can contribute to the development of skin cancer and alter host resistance to infectious diseases. These findings have led to the development of a new field of research, termed photoimmunology, which is concerned with the effects of UV radiation on immunological processes. Our interest in this field arose from studies on the antigenic properties of skin cancers induced in mice by chronic exposure to UV-B (280-320 nm) radiation. These cancers are highly antigenic and many are immunologically rejected upon transplantation to normal syngeneic recipients. In studying how these cancers were able to survive and grow in the primary host, we discovered that exposing the skin to UV radiation altered some types of immune responses, including the immune response against skin cancers. Studies on the nature and mechanism of the immunological alterations brought about by exposure to UV radiation suggested that UV-induced DNA damage triggers a cascade of events, leading ultimately to a state of antigen-specific, systemic T lymphocyte-mediated immunosuppression. Key components of this cascade are epidermal cytokines, which modulate the immune response to antigens introduced into the UV-irradiated host and divert the response toward a state of specific immunosuppression. The finding that UV radiation can redirect the immune response from an effector to a suppressor pathway has raised the possibility that immune responses to infectious diseases might also be influenced by exposure of the host to UV radiation. Interest in the health consequences of stratospheric ozone depletion, with its attendant increase in solar UV-B radiation, has stimulated recent investigations on the effects of UV radiation on the pathogenesis of infections in animal models and on immune responses in humans. In addition, attempts are being made to use information about UV-induced specific immunosuppression to eliminate unwanted immune responses, such as transplant rejection and graft-versus-host reactions. Thus, studies on the immunological effects of UV radiation are providing new information on how immune responses are regulated as well as improving our understanding of the role of the immune system in skin cancer induction. This information should facilitate the development of more effective measures for preventing the deleterious effects of overexposure to UV radiation.
太阳辐射的致癌活性已为人所知近一个世纪。然而，在过去几年里，我们意识到让皮肤暴露在阳光下对宿主也有深远的免疫影响，而且这些免疫变化会促使皮肤癌的发生，并改变宿主对传染病的抵抗力。这些发现催生了一个新的研究领域，即光免疫学，该领域关注紫外线辐射对免疫过程的影响。我们对这个领域的兴趣源于对长期暴露于UV-B（280 - 320纳米）辐射下的小鼠诱发的皮肤癌抗原特性的研究。这些癌症具有高度抗原性，许多在移植到同基因正常受体后会被免疫排斥。在研究这些癌症如何在原发宿主中存活和生长时，我们发现让皮肤暴露于紫外线辐射会改变某些类型的免疫反应，包括针对皮肤癌的免疫反应。对紫外线辐射引起的免疫改变的性质和机制的研究表明，紫外线诱导的DNA损伤引发了一系列事件，最终导致抗原特异性的、全身性T淋巴细胞介导的免疫抑制状态。这个级联反应的关键成分是表皮细胞因子，它们调节对引入紫外线照射宿主的抗原的免疫反应，并将反应导向特异性免疫抑制状态。紫外线辐射能将免疫反应从效应途径重定向到抑制途径这一发现，增加了宿主暴露于紫外线辐射也可能影响对传染病的免疫反应的可能性。对平流层臭氧消耗及其伴随的太阳UV-B辐射增加对健康影响的关注，激发了近期关于紫外线辐射对动物模型中感染发病机制和人类免疫反应影响的研究。此外，人们正在尝试利用紫外线诱导的特异性免疫抑制信息来消除不必要的免疫反应，如移植排斥和移植物抗宿主反应。因此，关于紫外线辐射免疫效应的研究正在提供有关免疫反应如何被调节的新信息，同时增进我们对免疫系统在皮肤癌诱发中作用的理解。这些信息应有助于制定更有效的措施来预防过度暴露于紫外线辐射的有害影响。
